Christopher M. Gomez to Animals
This is a "connection" page, showing publications Christopher M. Gomez has written about Animals.
Connection Strength
0.671
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a1ACT Is Essential for Survival and Early Cerebellar Programming in a Critical Neonatal Window. Neuron. 2019 05 22; 102(4):770-785.e7.
Score: 0.041
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The cerebellum in health and disease. Neurosci Lett. 2019 01 01; 688:1.
Score: 0.039
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Targeting the CACNA1A IRES as a Treatment for Spinocerebellar Ataxia Type 6. Cerebellum. 2018 02; 17(1):72-77.
Score: 0.038
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Spinocerebellar [corrected] Ataxia Type 6: Molecular Mechanisms and Calcium Channel Genetics. Adv Exp Med Biol. 2018; 1049:147-173.
Score: 0.038
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Mammalian Polycistronic mRNAs and Disease. Trends Genet. 2017 02; 33(2):129-142.
Score: 0.035
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An miRNA-mediated therapy for SCA6 blocks IRES-driven translation of the CACNA1A second cistron. Sci Transl Med. 2016 07 13; 8(347):347ra94.
Score: 0.034
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Revelations from a bicistronic calcium channel gene. Cell Cycle. 2014; 13(6):875-6.
Score: 0.029
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Selective inhibition of caspases in skeletal muscle reverses the apoptotic synaptic degeneration in slow-channel myasthenic syndrome. Hum Mol Genet. 2014 Jan 01; 23(1):69-77.
Score: 0.028
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Second cistron in CACNA1A gene encodes a transcription factor mediating cerebellar development and SCA6. Cell. 2013 Jul 03; 154(1):118-33.
Score: 0.028
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Skeletal muscle calpain acts through nitric oxide and neural miRNAs to regulate acetylcholine release in motor nerve terminals. J Neurosci. 2013 Apr 24; 33(17):7308-7324.
Score: 0.027
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Further evidence for the role of IP 3R 1 in regulating subsynaptic gene expression and neuromuscular transmission. Channels (Austin). 2012 Jan-Feb; 6(1):65-8.
Score: 0.025
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Skeletal muscle IP3R1 receptors amplify physiological and pathological synaptic calcium signals. J Neurosci. 2011 Oct 26; 31(43):15269-83.
Score: 0.025
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Calpain activation impairs neuromuscular transmission in a mouse model of the slow-channel myasthenic syndrome. J Clin Invest. 2007 Oct; 117(10):2903-12.
Score: 0.019
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Molecular pathogenesis of spinocerebellar ataxia type 6. Neurotherapeutics. 2007 Apr; 4(2):285-94.
Score: 0.018
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Inositol-1,4,5-triphosphate receptors mediate activity-induced synaptic Ca2+ signals in muscle fibers and Ca2+ overload in slow-channel syndrome. Cell Calcium. 2007 Apr; 41(4):343-52.
Score: 0.017
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Activation of apoptotic pathways at muscle fiber synapses is circumscribed and reversible in a slow-channel syndrome model. Neurobiol Dis. 2006 Aug; 23(2):462-70.
Score: 0.017
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C-termini of P/Q-type Ca2+ channel alpha1A subunits translocate to nuclei and promote polyglutamine-mediated toxicity. Hum Mol Genet. 2006 May 15; 15(10):1587-99.
Score: 0.017
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Translational Neuroscience: a Neurologist's translation. Curr Neurol Neurosci Rep. 2006 Mar; 6(2):85-7.
Score: 0.017
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Expression of Semaphorin-3A and its receptors in endochondral ossification: potential role in skeletal development and innervation. Dev Dyn. 2005 Oct; 234(2):393-403.
Score: 0.016
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Active calcium accumulation underlies severe weakness in a panel of mice with slow-channel syndrome. J Neurosci. 2002 Aug 01; 22(15):6447-57.
Score: 0.013
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The Transcription Factor, a1ACT, Acts Through a MicroRNA Network to Regulate Neurogenesis and Cell Death During Neonatal Cerebellar Development. Cerebellum. 2023 Aug; 22(4):651-662.
Score: 0.013
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Novel delta subunit mutation in slow-channel syndrome causes severe weakness by novel mechanisms. Ann Neurol. 2002 Jan; 51(1):102-12.
Score: 0.013
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Loss-of-function BK channel mutation causes impaired mitochondria and progressive cerebellar ataxia. Proc Natl Acad Sci U S A. 2020 03 17; 117(11):6023-6034.
Score: 0.011
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Genetic manipulation of AChR responses suggests multiple causes of weakness in slow-channel syndrome. Ann N Y Acad Sci. 1998 May 13; 841:167-80.
Score: 0.010
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Desensitization of mutant acetylcholine receptors in transgenic mice reduces the amplitude of neuromuscular synaptic currents. Synapse. 1997 Dec; 27(4):367-77.
Score: 0.009
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Slow-channel transgenic mice: a model of postsynaptic organellar degeneration at the neuromuscular junction. J Neurosci. 1997 Jun 01; 17(11):4170-9.
Score: 0.009
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A transgenic mouse model of the slow-channel syndrome. Muscle Nerve. 1996 Jan; 19(1):79-87.
Score: 0.008
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DnaJ-1 and karyopherin a3 suppress degeneration in a new Drosophila model of Spinocerebellar Ataxia Type 6. Hum Mol Genet. 2015 Aug 01; 24(15):4385-96.
Score: 0.008
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Fluoxetine is neuroprotective in slow-channel congenital myasthenic syndrome. Exp Neurol. 2015 Aug; 270:88-94.
Score: 0.008
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WDR81 is necessary for purkinje and photoreceptor cell survival. J Neurosci. 2013 Apr 17; 33(16):6834-44.
Score: 0.007
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Stable respiratory activity requires both P/Q-type and N-type voltage-gated calcium channels. J Neurosci. 2013 Feb 20; 33(8):3633-45.
Score: 0.007
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Frequency of KCNC3 DNA variants as causes of spinocerebellar ataxia 13 (SCA13). PLoS One. 2011 Mar 29; 6(3):e17811.
Score: 0.006
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Spinocerebellar ataxia type 6 knockin mice develop a progressive neuronal dysfunction with age-dependent accumulation of mutant CaV2.1 channels. Proc Natl Acad Sci U S A. 2008 Aug 19; 105(33):11987-92.
Score: 0.005
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Chronic experimental autoimmune myasthenia gravis induced by monoclonal antibody to acetylcholine receptor: biochemical and electrophysiologic criteria. J Immunol. 1987 Jul 01; 139(1):73-6.
Score: 0.005
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Novel beta subunit mutation causes a slow-channel syndrome by enhancing activation and decreasing the rate of agonist dissociation. Mol Cell Neurosci. 2006 May-Jun; 32(1-2):82-90.
Score: 0.004
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Monoclonal anti-acetylcholine receptor antibodies with differing capacities to induce experimental autoimmune myasthenia gravis. J Immunol. 1985 Jul; 135(1):234-41.
Score: 0.004
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Induction of the morphologic changes of both acute and chronic experimental myasthenia by monoclonal antibody directed against acetylcholine receptor. Acta Neuropathol. 1984; 63(2):131-43.
Score: 0.004
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Anti-acetylcholine receptor antibodies directed against the alpha-bungarotoxin binding site induce a unique form of experimental myasthenia. Proc Natl Acad Sci U S A. 1983 Jul; 80(13):4089-93.
Score: 0.003
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Monoclonal hybridoma anti-acetylcholine receptor antibodies: antibody specificity and effect of passive transfer. Ann N Y Acad Sci. 1981; 377:97-109.
Score: 0.003
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The polyglutamine expansion in spinocerebellar ataxia type 6 causes a beta subunit-specific enhanced activation of P/Q-type calcium channels in Xenopus oocytes. J Neurosci. 2000 Sep 01; 20(17):6394-403.
Score: 0.003
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The conserved RING-H2 finger of ROC1 is required for ubiquitin ligation. J Biol Chem. 2000 May 19; 275(20):15432-9.
Score: 0.003
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Antibody effector mechanisms in myasthenia gravis. The complement hypothesis. Ann N Y Acad Sci. 1998 May 13; 841:450-65.
Score: 0.002
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Effector mechanisms of myasthenic antibodies. Ann N Y Acad Sci. 1993 Jun 21; 681:264-73.
Score: 0.002
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Restricted use of T cell receptor V genes in murine autoimmune encephalomyelitis raises possibilities for antibody therapy. Cell. 1988 Aug 12; 54(4):577-92.
Score: 0.001
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Use of monoclonal antiacetylcholine receptor antibodies to investigate the macrophage inflammation of acute experimental myasthenia gravis: refractoriness to a second episode of acute disease. Neurology. 1985 Oct; 35(10):1455-60.
Score: 0.001
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Myasthenia induced by monoclonal anti-acetylcholine receptor antibodies: clinical and electrophysiological aspects. Ann Neurol. 1981 Jun; 9(6):563-8.
Score: 0.001
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Monoclonal anti-acetylcholine receptor antibodies can cause experimental myasthenia. Nature. 1980 Aug 14; 286(5774):738-9.
Score: 0.001